Harrison
Harrison
Harrison
Beth Harrison
Advisor: Samuel Powdrill, PA-C
PAS 646
Outline
Healthy Heart
Blood Flow
Deoxygenated blood from the body enters
the RA
At the same time, oxygen rich blood
leaves the lungs to flow into the LA
Blood in the RA enters the RV through the
tricuspid valve
At the same time, blood flows from the LA
to the LV through the mitral valve
ToF
4 anatomic
malformations:
-Right Ventricular
Hypertrophy
-Pulmonary Valve
Stenosis
-Transposition of
the aorta
-Ventricular Septal
Defect
ToF
RVH
-secondary to PA Stenosis
-Increased P on RV leads to RVH
Transposition of Aorta
-aorta is displaced
VSD
-hole in the heart
-mixing of oxygenated and unoxygenated blood
-cyanosis
PVS
-more severe, less blood transported to the lungs and
more deoxygenated blood will pass through VSD to
aorta to be circulated throughout the body
Etiology
Theory: destruction of the neuronal crest
cells during embryogenesis
In the laboratory setting, destruction of
these cells reproduced results displayed
with certain cardiac malformations.
Clinical Presentation
Clinical presentation is directly related to
the degree of pulmonary stenosis.
Severe stenosis results in immediate
cyanosis following birth. Mild stenosis will
not present until later.
Growth is retarded insufficient oxygen
and nutrients
SOA on exertion
Tet Spell
Tet spells at 23yo, child
becomes
cyanotic, may
experience
syncope
Surgical Intervention 1
Complete intracardiac repair of VSD and
PA stenosis.
Enter chest through the sternum. Connect
the heart and lung machine. Heart is
stopped.
Repair the VSD with a patch.
Determine if PA needs to be removed or if
removing the excessive muscle tissue will
help to function correctly.
Surgical Intervention 2
New method for patching the VSD
Transcatheter patches were selected
specifically for VSD size. Radio-opaque
loop inside of each patch allowed for
attachment of double nylon thread. Made
retrieval possible if necessary.
Pts were anticoagulated with heparin
initially, followed with ASA 24 hr later.
References